Estudo confirma ligação entre implantes mamários e forma rara de câncer

Implantes e linfoma

Os implantes de mama estão associados com uma forma rara de linfoma, de acordo com um estudo realizado por pesquisadores da RAND Corporation.

O estudo também descobriu que a doença tem uma evolução lenta e pode ser controlada pela remoção cirúrgica da cápsula do implante.

Apesar disso, os cientistas afirmam que ainda não há provas de que o câncer seja causado diretamente pelos implantes - eles ainda não compreendem o mecanismo de desenvolvimento da doença.

Ou seja, o estudo mostra que os dois - implantes e linfoma - ocorrem juntos, sem estabelecer uma relação causal. Mas a eliminação do implante parece ser o melhor tratamento para a doença.

Linfoma anaplásico de grandes células

As conclusões são baseadas em uma revisão exaustiva da literatura médica sobre os implantes mamários e o linfoma anaplásico de grandes células, ou ALCL, um tipo de câncer do sistema imunológico.

Os pesquisadores também discutiram os resultados da literatura médica com um painel multidisciplinar de especialistas.

A ligação entre o ALCL e os implantes mamários foi sugerida há mais de uma década.

Câncer muito raro

As preocupações sobre uma associação entre os implantes de mama e o linfoma anaplásico de grandes células foram levantadas pela primeira vez em 1996, quando médicos publicaram um relatório que descrevia uma mulher com implantes que tinham desenvolvido o câncer no tecido situado junto a um de seus implantes.

Desde aquela época, relatos semelhantes foram publicados, estimando-se que cerca de 1 a 3 casos seriam diagnosticados anualmente por milhão de mulheres com implantes.

Devido a essas preocupações crescentes, a Fundação de Cirurgia Plástica e a Fundação de Pesquisas e Educação em Cirurgia Estética, entidades dos profissionais da área, encomendaram à RAND uma revisão exaustiva da literatura médica e a organização de um painel de médicos especialistas para avaliar a existência de um vínculo potencial entre implantes mamários e ALCL e as suas implicações.

Retira do implante

Foram identificados 36 casos publicados de linfoma não-Hodgkin entre mulheres com implantes mamários, dos quais 29 foram diagnosticados como linfoma anaplásico de grandes células.

Pelo menos 12 das 29 mulheres tinham um histórico prévio de um tipo diferente de câncer, incluindo oito que haviam sido mastectomizadas por câncer de mama e duas que tinham um histórico anterior de ALCL.

Não houve nenhuma evidência de que fatores de risco da paciente ou de determinados tipos de implantes aumentem o risco da doença.

Enquanto algumas pacientes receberam quimioterapia e ou radioterapia, o tratamento na maioria dos casos consistiu da remoção cirúrgica do implante afetado e dos tecidos circundantes, o que apareceu ser o suficiente para controlar a doença.

Não houve óbitos entre as 16 mulheres para as quais estavam disponíveis informações de acompanhamento.

Fracassa mais um teste de vacina contra a AIDS

Tropeços

Fracassou mais uma tentativa de encontrar uma vacina contra o HIV.

O anúncio da suspensão precoce dos testes foi feito depois que estudos preliminares mostraram que não havia diferenças entre os grupos de controle e os grupos que tomaram o candidato a novo medicamento.

O estudo começou em Julho de 2009, e sua suspensão repentina surpreendeu os pesquisadores de todo o mundo, dadas as expectativas promissoras dos testes.

É o segundo revés importante na área, depois que uma vacina múltipla contra a AIDS produziu resultados modestos, em 2009.

Truvada

O teste consistia em doses diárias de um medicamento chamado Truvada, que contém duas drogas antirretrovirais.

Uma pesquisa internacional, com participação de brasileiros, havia demonstrado no ano passado que o Truvada poderia funcionar como uma vacina contra o vírus da AIDS.

Isto é o que os cientistas chamam de profilaxia de pré-exposição. Um teste anterior do Truvada misturado a um gel vaginal também havia dado resultados promissores, levando a crer que ele poderia prevenir a transmissão da AIDS.

Mas não foi isso o que as estatísticas mostraram.

Tanto faz

O estudo envolvia cerca de 2.000 mulheres na África do Sul, Tanzânia e Quênia.

No total, 56 mulheres foram infectadas durante esta etapa preliminar, metade das quais estava recebendo o medicamento - a outra metade estava recebendo placebo.

Há ainda dúvidas sobre se as mulheres estavam mesmo tomando o medicamento, embora, no conjunto, elas relatassem fazê-lo em 95% do tempo. Os cientistas coletaram amostras de sangue e vão analisar o conteúdo da droga no sangue para comparar com os relatos.

Estratégias para vacina contra a AIDS

O estudo estava sendo conduzido pela Family Health International (FHI) uma entidade sem fins lucrativos dos Estados Unidos.

A entidade decidiu encerrar prematuramente os testes do medicamento depois que observadores independentes atestaram que não haveria base estatística para demonstrar uma eventual eficácia do Truvada.

Em visita ao Brasil neste mês de Abril, David Watkins, um dos maiores especialistas do mundo em vacinas, afirmou que os cientistas estão mudando a estratégia para o desenvolvimento de uma vacina contra o HIV.

• Vacina anti-HIV: mito ou realidade?

Biophysicist Targeting IL-6 to Halt Breast, Prostate Cancer

ScienceDaily (Apr. 19, 2011) — An Ohio State biophysicist used a supercomputer to search thousands of molecular combinations for the best configuration to block a protein that can cause breast or prostate cancer.

An electrostatic representation (red: negative; blue: positive; white: hydrophobic) created at the Ohio Supercomputer Center by Ohio State’s Chenglong Li, Ph.D., shows IL-6 in ribbon representation. The two larger yellow ellipses indicate the two binding "hot spots" between IL-6 and GP130, key to blocking a protein that plays a role in breast and prostate cancer. (

Chenglong Li, Ph.D., an assistant professor of medicinal chemistry and pharmacognosy at The Ohio State University (OSU), is leveraging a powerful computer cluster at the Ohio Supercomputer Center (OSC) to develop a drug that will block the small protein molecule Interleukin-6 (IL-6). The body normally produces this immune-response messenger to combat infections, burns, traumatic injuries, etc. Scientists have found, however, that in people who have cancer, the body fails to turn off the response and overproduces IL-6.

"There is an inherent connection between inflammation and cancer," explained Li. "In the case of breast cancers, a medical review systematically tabulated IL-6 levels in various categories of cancer patients, all showing that IL-6 levels elevated up to 40-fold, especially in later stages, metastatic cases and recurrent cases."

In 2002, Japanese researchers found that a natural, non-toxic molecule created by marine bacteria -- madindoline A (MDL-A) -- could be used to mildly suppress the IL-6 signal. Unfortunately, the researchers also found the molecule wouldn't bind strongly enough to be effective as a cancer drug and would be too difficult and expensive to synthesize commercially. And, most surprisingly, they found the bacteria soon mutated to produce a different, totally ineffectual compound. Around the same time, Stanford scientists were able to construct a static image of the crystal structure of IL-6 and two additional proteins.

Li recognized the potential of these initial insights and partnered last year with an organic chemist and a cancer biologist at OSU's James Cancer Hospital to further investigate, using an OSC supercomputer to construct malleable, three-dimensional color simulations of the protein complex.

"The proximity of two outstanding research organizations -- the James Cancer Hospital and OSC -- provide a potent enticement for top medical investigators, such as Dr. Li, to conduct their vital computational research programs at Ohio State University," said Ashok Krishnamurthy, interim co-executive director of OSC.

"We proposed using computational intelligence to re-engineer a new set of compounds that not only preserve the original properties, but also would be more potent and efficient," Li said. "Our initial feasibility study pointed to compounds with a high potential to be developed into a non-toxic, orally available drug."

Li accessed 64 nodes of OSC's Glenn IBM 1350 Opteron cluster to simulate IL-6 and the two additional helper proteins needed to convey the signal: the receptor IL-6R and the common signal-transducing receptor GP130. Two full sets of the three proteins combine to form a six-sided molecular machine, or "hexamer," that transmits the signals that will, in time, cause cellular inflammation and, potentially, cancer.

Li employed the AMBER (Assisted Model Building with Energy Refinement) and AutoDock molecular modeling simulation software packages to help define the interactions between those proteins and the strength of their binding at five "hot spots" found in each half of the IL-6/IL-6R/GP130 hexamer.

By plugging small molecules, like MDL-A, into any of those hot spots, Li could block the hexamer from forming. So, he examined the binding strength of MDL-A at each of the hexamer hotspots, identifying most promising location, which turned out to be between IL-6 and the first segment, or modular domain (D1), of the GP130.

To design a derivative of MDL-A that would dock with D1 at that specific hot spot, Li used the CombiGlide screening program to search through more than 6,000 drug fragments. So far, he has identified two potential solutions by combining the "top" half of the MDL-A molecule with the "bottom" half of a benzyl molecule or a pyrazole molecule. These candidates preserve the important binding features of the MDL-A, while yielding molecules with strong molecular bindings that also are easier to synthesize than the original MDL-A.

"While we didn't promise to have a drug fully developed within the two years of the project, we're making excellent progress," said Li. "The current research offers us an exciting new therapeutic paradigm: targeting tumor microenvironment and inhibiting tumor stem cell renewal, leading to a really effective way to overcome breast tumor drug resistance, inhibiting tumor metastasis and stopping tumor recurrence."

While not yet effective enough to be considered a viable drug, laboratory tests on tissue samples have verified the higher potency of the derivatives over the original MDL-A. Team members are preparing for more sophisticated testing in a lengthy and carefully monitored evaluation process.

Li's project is funded by a grant from the Department of Defense (CDMRP grant number BC095473) and supported by the award of an OSC Discovery Account. The largest funding areas of Congressionally Directed Medical Research Programs (CDMRP) are breast cancer, prostate cancer and ovarian cancer. Another Defense CDMRP grant involving Li supports a concurrent OSU investigation of the similar role that IL-6 plays in causing prostate cancer. Those projects are being conducted in collaboration with Li's Medicinal Chemistry colleague, Dr. James Fuchs, as well as Drs. Tushar Patel, Greg Lesinski and Don Benson at OSU's College of Medicine and James Cancer Hospital, and Dr. Jiayuh Lin at Nationwide Children's Hospital in Columbus.

"In addition to leading the center's user group this year, the number and depth of Dr. Li's computational chemistry projects have ranked him one of our most prolific research clients," Krishnamurthy noted.

Decoding Human Genes Is Goal of New Open-Source Encyclopedia

ScienceDaily (Apr. 19, 2011) — A massive database cataloging the human genome's functional elements -- including genes, RNA transcripts, and other products -- is being made available as an open resource to the scientific community, classrooms, science writers, and the public, thanks to an international team of researchers.

ENCODE is a massive database cataloging many of the functional elements of the entire collection of human genes -- the human genome. The ENCODE data are being made available to the scientific community and to the public as an open resource, thanks to an international team of researchers. This illustration shows a group of proteins in the process of traveling along a spiraling strand of DNA, a structure comprised of genetic material. A chromosome structure, composed of tightly coiled DNA, is illustrated in the background.

In a paper that will be published in the journal PLoS Biology on 19 April 2011, the project -- called ENCODE (Encyclopedia Of DNA Elements) -- provides an overview of the team's ongoing efforts to interpret the human genome sequence, as well as a guide for using the vast amounts of data and resources produced so far by the project.

Ross Hardison, the T. Ming Chu Professor of Biochemistry and Molecular Biology at Penn State University and one of the principal investigators of the ENCODE Project team, explained that the philosophy behind the project is one of scientific openness, transparency, and collaboration across sub-disciplines. ENCODE comes on the heels of the now-complete Human Genome Project -- a 13-year effort aimed at identifying all the approximately 20,000 to 25,000 genes in human DNA -- which also was based on the belief in open-source data sharing to further scientific discovery and public understanding of science.

The ENCODE Project has accomplished this goal by publishing its database at genome.ucsc.edu/ENCODE, and by posting tools to facilitate data use at encodeproject.org. "ENCODE resources are already being used by scientists for discovery," Hardison said. "But what's kind of revolutionary is that they also are being used in classes to train students in all areas of biology. Our classes here at Penn State are using real data on genomic variation and function in classroom problem sets, shortly after the labs have generated them."

Hardison explained that there are about 3-billion base pairs in the human genome, making the cataloging and interpretation of the information a monumental task. "We have a very lofty goal: To identify the function of every nucleotide of the human genome," he said. "Not only are we discovering the genes that give information to cells and make proteins, but we also want to know what determines that the proteins are made in the right cells, and at the appropriate time. Finding the DNA elements that govern this regulated expression of genes is a major goal of ENCODE." Hardison explained that ENCODE's job is to identify the human genome's functional regions, many of which are quite esoteric. "The human DNA sequence often is described as a kind of language, but without a key to interpret it, without a full understanding of the 'grammar,' it might as well be a big jumble of letters." Hardison added that the ENCODE Project supplies data such as where proteins bind to DNA and where parts of DNA are augmented by additional chemical markers. These proteins and chemical additions are keys to understanding how different cells within the human body interpret the language of DNA.

In the soon-to-be-published paper, the team shows how the ENCODE data can be immediately useful in interpreting associations between disease and DNA sequences that can vary from person to person -- single nucleotide polymorphisms (SNPs). For example, scientists know that DNA variants located upstream of a gene called MYC are associated with multiple cancers, but until recently the mechanism behind this association was a mystery. ENCODE data already have been used to confirm that the variants can change binding of certain proteins, leading to enhanced expression of the MYC gene and, therefore, to the development of cancer. ENCODE also has made similar studies possible for thousands of other DNA variants that may be associated with susceptibility to a variety of human diseases.

Another of the principal investigators of the project, Richard Myers, president and director of the HudsonAlpha Institute for Biotechnology, explained that the ENCODE Project is unique because it requires collaboration from multiple people all over the world at the cutting edge of their fields. "People are working in a coordinated manner to figure out the function of our human genome," he said. "The importance of the project extends beyond basic knowledge of who and what we are as humans, and into an understanding of human health and disease."

Scientists with the ENCODE Project also are applying up to 20 different tests in 108 commonly used cell lines to compile important data. John Stamatoyannopoulos, an assistant professor of genome sciences and medicine at the University of Washington and another principal investigator, explained that the ENCODE Project has been responsible for producing many assays -- molecular-biology procedures for measuring the activity of biochemical agents -- that are now fundamental to biology. "Widely used computational tools for processing and interpreting large-scale functional genomic data also have been developed by the project," Stamatoyannopoulos added. "The depth, quality, and diversity of the ENCODE data are unprecedented."

Hardison said that the portion of the human genome that actually codes for protein is about 1.1 percent. "That's still a lot of data," he said. "And to complicate matters even more, most mechanisms for gene expression and regulation lie outside what we call the 'coding' region of DNA." Hardison explained that scientists have a limited number of tools with which to explore the genome, and one that has been used widely is inter-species comparison. "For example, we can compare humans and chimpanzees and glean some fascinating information," Hardison said. "But very few proteins and other DNA products differ in any fundamental way between humans and chimps. The important difference between us and our close cousins lies in gene expression -- the basic level at which genes give rise to traits such as eye color, height, and susceptibility to a particular disease. ENCODE is helping to map the very proteins involved in gene regulation and gene expression. Our paper not only explains how to find the data, but it also explains how to apply the data to interpret the human genome."

The ENCODE Project is funded, primarily, by the National Human Genome Research Institute of the U. S. National Institutes of Health.

Small Molecules Inhibit Growth of Human Tumor Cells

ScienceDaily (Apr. 19, 2011) — Researchers from the Cancer Institute at NYU Langone Medical Center have identified three novel small molecules that interrupt a crucial cellular communication pathway that regulates many aspects of development and cancer. The finding, published in the April 12, 2011 issue of the Proceedings of the National Academy of Sciences and featured on its cover, could provide the basis for innovative therapies for colorectal cancer and other diseases associated with aberrations in this pathway.

The impact of a small molecule that inhibits the Wnt pathway is shown in these panels of cultured cells seen under a microscope. Normal mouse mammary epithelial cells (panel 1) change shape when treated with Wnt-3a, a secreted molecule that activates the Wnt pathway (panel 2). Transformation of these cells can be blocked by a molecule called iCRT14 (panel 3). The cells are stained with β catenin (in red), filamentous actin (in green) and DAPI (nuclear stain in blue). (Credit: 

"Our study demonstrates that the three newly identified compounds are capable of blocking cell proliferation in cancerous human tumor biopsy cells," said Ramanuj DasGupta, PhD, assistant professor of Pharmacology at NYU School of Medicine and the NYU Cancer Institute, and the scientific director of the NYU RNAi Core Screening Facility.

Dr. DasGupta and his colleagues identified the molecules as inhibitors of the Wnt signaling pathway. This pathway is of special interest to scientists because it controls many biological processes by promoting cell-to-cell communication. Many previous studies have shown that cancers in the liver, breast, skin, and especially the colon, are associated with abnormal signaling activity in this pathway. However, it has been difficult to find potential therapeutic agents aimed at the Wnt pathway.

"These molecules hold a lot of promise towards future Wnt-based drug development for cancer treatments," says Dr. DasGupta. "They may allow the compounds to be used for specific therapeutic purposes in humans to induce the death of Wnt-dependent or Wnt -addicted cancer cells and tumor tissues without affecting the growth and proliferation of normal healthy cells."

The scientists demonstrated that the molecules suppressed the activity of the Wnt signaling pathway -- without disrupting other cellular functions -- in human colon cancers from biopsies, in colon cancer cell lines, and in a mouse tumor-xenograft model. In all instances, the inhibitors stopped the proliferation of cancerous cells in the laboratory dish or in the mouse.

"To date, no therapies for the control of Wnt-driven tumors have been available for colon cancer, lung cancer, leukemia, and other forms of the disease caused by mutations in the Wnt pathway," said Robert A. Nagourney, MD, of Rational Therapeutics in Long Beach, California, who is one of the study's authors. "The findings in our human tissue model give us real hope that these compounds will have important implications in future clinical therapy and the development of an effective Wnt inhibitor."

The Wnt pathway is complex and only partially understood. Wnt genes bind to receptors on the surface of cells, provoking a reaction (or a "signaling cascade") within the cell that ultimately allows various "downstream effector proteins" to go into action. One of these proteins, called β catenin, moves into the nucleus and oversees the activation of genes often associated with cell proliferation and other processes.

In the study, the researchers used an innovative, integrated screening platform combining RNA interference (RNAi) -technology and high-throughput chemical genetic screening to examine the potency of 14,977 compounds on the activity of the Wnt pathway. This targeted screening methodology helped identify the three promising novel inhibitors capable of blocking Wnt target genes in various mammalian cancer cell lines including human colon and breast cancer cells. Foster C. Gonsalves, PhD, first author of the study and post-doctoral fellow in Dr. DasGupta's lab, helped develop this technique.

"While more exploratory research of these promising compounds is needed, these small molecules identified in the RNAi screens can serve as prototypes for the development of future antitumor drugs targeting the Wnt signaling pathway in different Wnt-associated cancers," says Dr. DasGupta. "Similar RNAi-based integrated screening technology should be widely applicable to a variety of other signaling pathways implicated in human disease."

This study highlights the strength of high-throughput RNAi-based genome-wide or genome-scale modifier screens currently being performed at NYU's RNAi Screening Facility, according to Dr. DasGupta. The state-of-the-art functional genomic approach continues to help answer basic biological questions in cellular signaling and better define the Wnt pathway, he says.

Along with Dr. DasGupta and Dr. Gonsalves, the authors of the study include Keren Klein, Shauna Katz and Timothy Cardozo from NYU School of Medicine, and Brittany B. Carson and Anthony C. Brown from Weill Cornell Medical College.

The study was supported by grants from the National Institutes of Health, the Department of Defense, and The Helen L. and Martin S. Kimmel Center for Stem Cell Biology at NYU School of Medicine.

Limiting Carbs, Not Calories, Reduces Liver Fat Faster, Researchers Find

ScienceDaily (Apr. 19, 2011) — Curbing carbohydrates is more effective than cutting calories for individuals who want to quickly reduce the amount of fat in their liver, report UT Southwestern Medical Center researchers.

"What this study tells us is that if your doctor says that you need to reduce the amount of fat in your liver, you can do something within a month," said Dr. Jeffrey Browning, assistant professor of internal medicine at UT Southwestern and the study's lead author.

The results, available online and in an upcoming issue of the American Journal of Clinical Nutrition, could have implications for treating numerous diseases including diabetes, insulin resistance and nonalcoholic fatty liver disease, or NAFLD. The disease, characterized by high levels of triglycerides in the liver, affects as many as one-third of American adults. It can lead to liver inflammation, cirrhosis and liver cancer.

For the study, researchers assigned 18 participants with NAFLD to eat either a low-carbohydrate or a low-calorie diet for 14 days.

The participants assigned to the low-carb diet limited their carbohydrate intake to less than 20 grams a day -- the equivalent of a small banana or a half-cup of egg noodles -- for the first seven days. For the final seven days, they switched to frozen meals prepared by UT Southwestern's Clinical and Translational Research Center (CTRC) kitchen that matched their individual food preferences, carbohydrate intake and energy needs.

Those assigned to the low-calorie diet continued their regular diet and kept a food diary for the four days preceding the study. The CTRC kitchen then used these individual records to prepare all meals during the 14-day study. Researchers limited the total number of calories to roughly 1,200 a day for the female participants and 1,500 a day for the males.

After two weeks, researchers used advanced imaging techniques to analyze the amount of liver fat in each individual. They found that the study participants on the low-carb diet lost more liver fat.

Although the study was not designed to determine which diet was more effective for losing weight, both the low-calorie dieters and the low-carbohydrate dieters lost an average of 10 pounds.

Dr. Browning cautioned that the findings do not explain why participants on the low-carb diet saw a greater reduction in liver fat, and that they should not be extrapolated beyond the two-week period of study.

"This is not a long-term study, and I don't think that low-carb diets are fundamentally better than low-fat ones," he said. "Our approach is likely to be only of short-term benefit because at some point the benefits of weight loss alone trounce any benefits derived from manipulating dietary macronutrients such as calories and carbohydrates.

"Weight loss, regardless of the mechanism, is currently the most effective way to reduce liver fat."

Other UT Southwestern researchers involved in the study were Dr. Shawn Burgess, senior author and assistant professor of pharmacology in the Advanced Imaging Research Center (AIRC); Dr. Jonathan Baker, assistant professor of pathology; Dr. Thomas Rogers, former professor of pathology; Jeannie Davis, clinical research coordinator in the AIRC; and Dr. Santhosh Satapati, postdoctoral researcher in the AIRC.

The National Institutes of Health supported the study.

Filters That Reduce ‘brain Clutter’ Identified

ScienceDaily (Apr. 19, 2011) — Until now, it has been assumed that people with conditions like ADHD, Tourette syndrome, obsessive compulsive disorder and schizophrenia -- all of whom characteristically report symptoms of "brain clutter" -- may suffer from anomalies in the brain's prefrontal cortex.

Colored stimuli shown to animals during trials. The area shaded in red represents the dorsolateral prefrontal cortex of the brain. 

Damage to this brain region is often associated with failure to focus on relevant things, loss of inhibitions, impulsivity and various kinds of inappropriate behaviour. So far, exactly what makes the prefrontal cortex so essential to these aspects of behaviour has remained elusive, hampering attempts to develop tools for diagnosing and treating these patients.

But new research by Julio Martinez-Trujillo, a professor in McGill University's Department of Physiology and Canada Research Chair in Visual Neuroscience, has brought new hope to these patients. He believes the key to the "brain clutter" and impulsivity shown by individuals with dysfunctional prefrontal cortices lies in a malfunction of a specific type of brain cell. Martinez-Trujilo and his team have identified neurons in the dorsolateral sub-region of the primate prefrontal cortex that selectively filter out important from unimportant visual information. The key to the normal functioning of these "filter neurons" is their ability to, in the presence of visual clutter, selectively and strongly inhibit the unimportant information, giving the rest of the brain access to what is relevant.

"Contrary to common beliefs, the brain has a limited processing capacity. It can only effectively process about one per cent of the visual information that it takes in," Martinez-Trujilo said. "This means that the neurons responsible for perceiving objects and programming actions must constantly compete with one another to access the important information.

"What we found when we looked at the behaviour of the neurons in the prefrontal cortex, was that an animal's ability to successfully accomplish a single action in the presence of visual clutter, was dictated by how well these units suppressed distracting information."

These results could be highly relevant for identifying the causes and improving the diagnosis and treatments of a wide range of mental disorders including ADHD and schizophrenia.

The research was conducted by Therese Lennert, a PhD student who holds a Vanier Scholarship, and it was funded by the Canada Research Chair program, Canadian Institutes of Health Research (CIHR), EJLB Foundation, and Natural Sciences and Engineering Research Council of Canada (NSERC).

More Accurate Diagnosis of Alzheimer’s

ScienceDaily (Apr. 19, 2011) — A new study from the University of Gothenburg, Sweden, shows how analysing spinal fluid can help to detect Alzheimer's disease at an early stage. The researchers behind the study hope that their findings will contribute to a greater international breakthrough for this type of diagnostic method.

It all comes down to biomarkers, substances that are found at abnormally high or low levels in patients who go on to develop Alzheimer's. The most common biomarkers to be identified by the researchers in the spinal fluid of patients with Alzheimer's are proteins and peptides -- short chains of amino acids.

"What's new about our study is that the biomarkers are really good, better than in the past, as the study was carried out extremely carefully with suitable participants via clinical trials and well implemented and controlled laboratory analyses," says docent Johan Svensson, who is working with professor Kaj Blennow's research group at the Sahlgrenska Academy, which has long been involved in researching the development of these biomarkers and advocating their use.

A total of 60 patients who were being investigated for dementia took part in the study, along with 20 healthy controls.

"We measured levels of the biomarkers in the spinal fluid and found that high levels of these substances confirmed the diagnosis of Alzheimer's with a high degree of accuracy compared with levels in healthy controls and patients with other forms of dementia," says Svensson.

"We also saw that patients who hadn't yet met all the clinical criteria for Alzheimer's had similar levels of the biomarkers in their spinal fluid to patients who had developed the disease fully."

The research group therefore concludes that these measurements can also be used to identify Alzheimer's during the early stages of the disease. In such cases, the biomarkers can be used to identify those patients with mild symptoms who are most likely to benefit from treatment.

"If a medication that affects the course of the disease does become available, it will probably be most effective during the early stages, and these biomarkers could be used in the development of such a medication," says Svensson.

The study will be published in the Journal of Alzheimer's Disease.